Endo - Physiology (Adrenal) Flashcards

Pg. 312-313 in First Aid 2014 Sections include: -Adrenal steroids and congenital adrenal hyperplasias -Cortisol

1
Q

What regulates cholesterol desmolase in the adrenal cortex, and how so?

A

ACTH stimulates, Ketoconazole inhibits

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2
Q

What reaction does cholesterol desmolase catalyze in the adrenal cortex? Towards what final product does this reaction contribute? Where is this produced?

A

Cholesterol –> Pregnenolone; Aldosterone; Zona Glomerulosa

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3
Q

What 3 reactions does 3Beta-hydroxysteroid dehydrogenase catalyze in the adrenal cortex? Towards what final product does each of these reactions contribute? Where are each of these final products produced?

A

(1) Pregnenolone => Progesterone; Aldosterone (Zona Glomerulosa) (2) 17-hydroxypregenolone => 17-hydroxyprogesterone; Cortisol (Zona Fasciculata) (3) Dehydroepiandrosterone (DHEA) => Androstenedione; Testosterone/Estradiol (Zona Reticularis)

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4
Q

What 2 reactions does 21-hydroxylase catalyze in the adrenal cortex? Towards what final product does each of these reactions contribute? Where are each of these final products produced?

A

(1) Progesterone => 11-deoxycorticosterone; Aldosterone (Zona Glomerulosa) (2) 17-hydroxyprogesterone => 11-deoxycortisol; Cortisol (Zona Fasciculata)

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5
Q

What 2 reactions does 11Beta-hydroxylase catalyze in the adrenal cortex? Towards what final product does each of these reactions contribute? Where is each produced?

A

(1) 11-deoxycorticosterone => corticosterone; Aldosterone (Zona Glomerulosa) (2) 11-deoxycortisol => Cortisol; Cortisol (Zona Fasciculata)

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6
Q

What reaction does Aldosterone synthase catalyze in the adrenal cortex? Towards what final product does this reaction contribute? Where is it produced?

A

Corticosterone => Aldosterone; Aldosterone (Zona Glomerulosa)

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7
Q

What regulates Aldosterone synthase in the adrenal cortex, and how?

A

Angiotensin II stimulates

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8
Q

What 2 reactions does 17alpha-hydroxylase catalyze in the adrenal cortex? Towards what final product does each of these reactions contribute? Where are each of these reactants and final products found?

A

(1) Pregenolone (Zona Glomerulosa) => 17-hydroxypregenolone (Zona Fasciculata) => Dehydroepiandrosterone (DHEA) (Zona Reticularis) (2) Progesterone (Zona Glomerulosa) => 17-hydroxyprogesterone (Zona Fasciculata) => Andostenedione (Zona Reticularis)

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9
Q

What type of substances is produced in each of the following zones of the adrenal cortex: (1) Zona Glomerulosa (2) Zona Fasciculata (3) Zona Reticularis?

A

(1) Mineralocorticoids (2) Glucocorticoids (3) Androgens

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10
Q

What is the progression of dihydroepiandrosterone (DHEA) to testosterone? Where does this occur in the adrenal cortex?

A

Dehydroepiandrosterone (DHEA) => Androstenedione => Testosterone; Zona Reticularis

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11
Q

What 3 sex hormones are produced in the peripheral tissue following conversion from a precursor in the adrenal cortex? What are each of their precursors, and what enzymes catalyze each of these reactions? Where in the adrenal cortex are all of the precursors located?

A

(1) Estrone; Aromatase coverts Androstenedione to Estrone (2) Estradiol; Aromatase converts Testosterone to Estradiol (3) Dihydrotestosterone (DHT); 5alpha-reductase converts Testosterone to Dihydrotestosterone (DHT)

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12
Q

In 17alpha-hydroxylase deficiency, how are the levels of each of the following changed: (1) Mineralcorticoids (2) Cortisol (3) Sex hormones.

A

(1) Increased (2) Decreased (3) Decreased

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13
Q

In 21-hydroxylase deficiency, how are the levels of each of the following changed: (1) Mineralcorticoids (2) Cortisol (3) Sex hormones.

A

(1) Decreased (2) Decreased (3) Increased

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14
Q

In 11beta-hydroxylase deficiency, how are the levels of each of the following changed: (1) Mineralcorticoids (2) Cortisol (3) Sex hormones.

A

(1) Decreased aldosterone, Increased 11-deoxycorticosterone (results in high BP) (2) Decreased (3) Increased

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15
Q

Again, what are the changes in mineralcorticoids in patients with 11beta-hydroxylase deficiency? Be specific. What effect does this have?

A

Decreased aldosterone, Increased 11-deoxycorticosterone (results in high BP)

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16
Q

What are 3 key lab findings that characterize 17alpha-hydroxylase deficiency?

A

(1) Hypertension (2) Hypokalemia (3) Low DHT

17
Q

What are 4 key lab findings that characterize 21-hydroxylase deficiency?

A

(1) Hypotension (2) Hyperkalemia (3) High renin activity (4) High 17-hydroxyprogesterone

18
Q

What 2 key lab findings characterize 11beta-hydroxylase deficiency, and why?

A

Hypertension (low renin)

19
Q

What changes occur to adrenal glands in response to congenital adrenal enzyme deficiencies, and why?

A

All congenital adrenal enzyme deficiencies are characterized by an enlargement of both adrenal glands due to increase ACTH stimulation (due to decreased cortisol).

20
Q

What is (are) the defining physical presentation(s) in patients with 17alpha-hydroxylase deficiency?

A

XY: pseudohermaphroditism (ambiguous genitalia, undescended testes); XY: lack secondary sexual development

21
Q

What is (are) the defining physical presentation(s) in patients with 21-hydroxylase deficiency?

A

Presents in infancy (salt wasting) or childhood (precious puberty); XX: virilization

22
Q

What is the defining physical presentation in patients with 11beta-hydroxylase deficiency?

A

XX: virilization

23
Q

What is the source of cortisol?

A

Adrenal zona fasciculata

24
Q

What are 6 major functions of cortisol?

A

(1) Increase blood pressure (upregulates alpha1-receptors on arterioles => increased sensitivity to norepinephrine and epineprhine) (2) Increase insulin resistance (diabetogenic) (3) Increase gluconeogenesis, lipolysis, and proteolysis (4) Decrease fibroblast activity (causing striae) (5) Decrease inflammatory and immune responses (A - inhibits production of leukotrienes and prostaglandins, B - Inhibits leukocyte adhesion => neutrophila, C - Blocks histamine release from mast cells, D - Reduces eosinophils, E - Blocks IL-2 production) (5) Decrease bone formation (decrease osteoblast activity); Think: “cortisol is a BIG FIB = Bp high, Insulin resistance, Gluconeogenesis etc., Fibroblast low, Inflammation/Immune low, Bone formation low.

25
Q

What effect can exogenous corticosteroids cause, and why?

A

Exogenous corticosteroids can cause reactivation of TB and candidiasis (blocked IL2 production)

26
Q

What causes the release of cortisol, and from where?

A

CRH (hypothalamus) stimulates ACTH release (pituitary), causing cortisol production in adrenal zona fasciculata

27
Q

What relationship does chronic stress have with cortisol?

A

Chronic stress induces prolonged secretion

28
Q

What hormonal/molecular effects does excess cortisol secretion have?

A

Excess cortisol decreases CRH, ACTH, and cortisol secretion